title: Innate type 2 immunity is associated with eosinophilic pleural effusion in primary spontaneous pneumothorax.
abstract: BACKGROUND
  Eosinophilic pleural effusion (EPE) is characterized by greater than 10% eosinophilia and is frequently associated with air and/or blood in the pleural cavity. Primary spontaneous pneumothorax (PSP), defined as the spontaneous presence of air in the pleural space, is one of the most common causes of EPE. Recent studies have shown that type 2 immune responses play important roles in eosinophilic airway inflammation resulting in pleural pathology.
  
  
  OBJECTIVE
  To determine the predominant immune responses associated with PSP in humans, and to examine whether IL-33, thymic stromal lymphopoietin (TSLP), or type 2 innate lymphoid cell (ILC2)-mediated immune responses are associated factors.
  
  
  METHODS
  Eosinophil-associated cytokines were measured in the pleural fluid of patients with PSP and control subjects. Th2 cell and ILC2 responses in the pleural cavity and peripheral blood were also evaluated by in vitro restimulation and intracellular cytokine staining of T cells and ILC2s in patients with PSP (n = 62) and control subjects (n = 33). IL-33-mediated IL-5 production by ILC2s was also evaluated.
  
  
  RESULTS
  Significantly higher concentrations of IL-5 and eotaxin-3 were detected in the pleural fluid of patients with PSP, in addition to significantly higher concentrations of IL-33 and TSLP. Although IL-5 production was induced by IL-33 treatment of ILC2s, other Th2 cell-mediated immune responses were not detected.
  
  
  CONCLUSIONS
  Our results indicate that innate immune responses characterized by the production of IL-33, TSLP, and IL-5 are associated with the development of EPE in PSP by an ILC2-dependent and Th2-independent mechanism.
authors.affiliation: Graduate School of Medical Science and Engineering, Biomedical Research Center, KAIST Institute for the BioCentury, Daejeon, Korea.
authors.forename: Bo-In
authors.initials: BI
authors.lastname: Kwon
authors.forename: Seokchan
authors.initials: S
authors.lastname: Hong
authors.forename: Kihyuk
authors.initials: K
authors.lastname: Shin
authors.forename: Eun-Hye
authors.initials: EH
authors.lastname: Choi
authors.forename: Jung-Joo
authors.initials: JJ
authors.lastname: Hwang
authors.forename: Seung-Hyo
authors.initials: SH
authors.lastname: Lee
mesh_terms: D000293:Adolescent; D001826:Body Fluids / Q000737:chemistry / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D016022:Case-Control Studies; D016207:Cytokines / Q000032:analysis; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D000067596:Interleukin-33; D007378:Interleukins / Q000032:analysis; D008297:Male; D008875:Middle Aged; D010996:Pleural Effusion / Q000209:etiology / Q000276:immunology*; D011030:Pneumothorax / Q000150:complications / Q000276:immunology*; D011657:Pulmonary Eosinophilia / Q000209:etiology / Q000276:immunology*; D000094632:Thymic Stromal Lymphopoietin
chemical_list: D016207:Cytokines; C506536:IL33 protein, human; D000067596:Interleukin-33; D007378:Interleukins; D000094632:Thymic Stromal Lymphopoietin